Evidence map›Paper›PMID 33929667›Full record

ArticleEnvironmental science and pollution research international2021

Pharmacological inhibition of HDAC1/3-interacting proteins induced morphological changes, and hindered the cell proliferation and migration of hepatocellular carcinoma cells.

Nouf Al-Yhya, Muhammad Farooq Khan, Rafa Sharaf Almeer, Mana M Alshehri, Mohammed S Aldughaim, Mohammad Ahmed Wadaan

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Article in Environmental science and pollution research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 10 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Nouf Al-YhyaDepartment of Zoology, College of Science, King Saud University, P.O. Box 2455, Riyadh, 11451, Saudi Arabia.
Muhammad Farooq KhanBio-products Research Chair, Department of Zoology, College of Science, King Saud University, P.O. Box 2455, Riyadh, 11451, Saudi Arabia. fmuhammad@ksu.edu.sa.ORCID http://orcid.org/0000-0001-9891-2443
Rafa Sharaf AlmeerDepartment of Zoology, College of Science, King Saud University, P.O. Box 2455, Riyadh, 11451, Saudi Arabia.
Mana M AlshehriKing Abdullah International Medical Research Center, King Saud Bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Ministry of National Guard Health Affairs, Riyadh, Saudi Arabia.
Mohammed S AldughaimResearch Center, King Fahad Medical City, P.O.BOX:59046, Riyadh, 1152, Saudi Arabia.
Mohammad Ahmed WadaanBio-products Research Chair, Department of Zoology, College of Science, King Saud University, P.O. Box 2455, Riyadh, 11451, Saudi Arabia.
King Saud University · SAKing Fahd Medical City · SAKing Saud bin Abdulaziz University for Health Sciences · SA

Funding

Deanship of Scientific Research, King Saud University Research chair program
6 · The paper itself

Abstract

Liver diseases are particularly severe health problems, but the options available for preventing and treating them remain limited. Accumulating evidence has shown that there is altered expression of individual histone deacetylase (HDAC) family members in hepatocellular carcinoma cells. In a previous study, we have identified a set of proteins which interact with histone deacetylase 1 and 3 (HDAC1/3) in hepatocellular carcinoma cell lines HepG2 by proteomic approach. This study was designed to investigate the therapeutic potential and expression of HDAC1/3-interacting genes in a human hepatocellular carcinoma cell line (HepG2). Pharmacological and transcriptional inhibition of HDAC1/3 resulted in the suppression of cancer cell proliferation, change of cell morphology, and downregulation of HDAC1/3 genes in HepG2 cells. The pharmacological inhibition also resulted in inhibition of liver cancer cell migration by wound scratch assay. Taken together, the results from this study show that the upregulation of HDAC1/3 in hepatocellular carcinoma resulted in the overexpression of CNOT1, PFDN2/6, and HMG20B, and that these genes could serve as novel molecular targets in liver cancer.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell LineCell Line, TumorCell ProliferationHep G2 CellsHigh Mobility Group ProteinsHistone Deacetylase 1Histone Deacetylase 3Histone DeacetylasesHumansMolecular ChaperonesProteomicsTranscription FactorsCNOT1 protein, humanHDAC1 protein, humanHigh Mobility Group ProteinsHistone Deacetylase 1Histone Deacetylase 3Histone DeacetylasesHMG20B protein, humanMolecular ChaperonesprefoldinTranscription FactorsHDAC1/3-interacting proteinsHepatocellular carcinomaHMG20BPFDNPrognostic biomarker in liver cancer

Identifiers

PMID33929667
OpenAlexW3157622415

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.